Abstract
Resting beat-to-beat blood pressure variability is a strong predictor of cardiovascular events and mortality. However, its underlying mechanisms remain incompletely understood. Given that the sympathetic nervous system plays a pivotal role in cardiovascular regulation, we hypothesized that alpha-1 adrenergic receptors (the main sympathetic receptor controlling peripheral vasoconstriction) may contribute to resting beat-to-beat blood pressure variability. Beat-to-beat heart rate (electrocardiography) and blood pressure (photoplethysmography) were continuously measured before and 2 h following, selective blockade of alpha-1 adrenergic receptors via oral administration of prazosin (1mg/20kg) in ten young healthy adults (two women). Cardiac output and total peripheral resistance were estimated using the ModelFlow method. Selective blockade of alpha-1 adrenergic receptors was confirmed by the marked reduction in the pressor response to intravenous infusion of phenylephrine hydrochloride (-80 ± 15%, P = 0.001 versus pre-prazosin). The blockade significantly decreased the standard deviation of the systolic (pre-prazosin versus post-prazosin: 5.6 ± 1.4 versus 3.8 ± 0.7mmHg, P = 0.002), diastolic (3.2 ± 1.2 versus 2.2 ± 0.5mmHg, P = 0.022), and mean blood pressure (3.7 ± 1.2 versus 2.5 ± 0.5mmHg, P = 0.009), as well as total peripheral resistance (0.8 ± 0.5 versus 0.5 ± 0.1mmHg/L/min, P = 0.047), but not cardiac output (521 ± 188 versus 453 ± 160mL/min, P = 0.321). Similar results were found using different indices of variability. These findings indicate that alpha-1 adrenergic receptors play a significant role in regulating resting beat-to-beat blood pressure variability in young, healthy adults.
Published Version
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